HEMS arrives on a patients where ground medical service is conducting a perfect ALS.

The 50 years old pt is in PEA cardiac arrest (CA) (sinus bradycardia narrow QRS) airway secured with an 8 ET. The pt was still pulseless (double checked) after almost 20 min of CA, 6 mg of epi already administered and good quality chest compression was ongoing. EtCO2 was 35 (!!!!) even when chest compression were stopped for the pulse check(!!!).

Still no palpable pulse. At this point a 12 lead EKG was performed (against alla the ALS dogmas) with the patient still pulseless and the chest compressions were conseguently suspended (other ALS eresia) while placing the precordial leads and acquiring the EKG.

S…t she is alive!!! This is not PEA but profound cardiogenic shock.

Pulseles Electric Activity a novel approach in medical cardiac arrest

When classical ALS algorithm comes to non defib rithm says that asystole and PEA are the same and have to be equally treated.

There is not such a clinical and therapeutic mistake.

Cardiac stand still and contractile cardiac activity without a palpable central pulse are totally different issues.Pulseless electric activity in the majority of cases is more like a profound state of shock than an asystole, and like this has to be treated.

But let’s make just a step backword.

First cosideration is on the identification of pulseless patients.

At the moment official guidelines consider a pulseless patient based on the palpation of carotid pulse. ERC BLS 2010 official guidelines about carotid pulse palpation says: “Checking the carotid pulse (or any other pulse) is an inaccurate method of confirming the presence or absence of circulation, both for lay rescuers and for professionals” so is no long recommended.

So why if is no recommended for BLS is used in ALS guidelines to recognize pulseless patients and to treat them as an asystolic one? Is our finger a reliable instrument to decide beetwen life and death? Even the BLS guidelines give us the answer: NO.

Second consideration is the research of the underlyng causes of PEA.

The H’s and T’s classification is an etiologic definition and not a clinical one and is often impossible to use in emergency settings cause of the lack of clinicla informations.

3 and 3 rule, even if still not validate, seems more helpful for clinicians working on the field or at least for quick use in emergency situation. On plus give us a guide for tretment according on patophisiologic origin of PEA.

The introduction of point of care echo and EtCO2 in ED and on the field put a new brick in definition, diagnosys and treatment of PEA.

Ultrasonography give us the chance to expolore, confirming or excluding, most of the mechanical causes of PEA and EtCO2 is a more reliable indicator of perfusion than the subjective pulse palpation.

Regarding the tretment options, there are still no evidences in favour or against epinephrine administation and chest compression utility in patients pulseless with electric activity and no cardiac standstill.

The end of clinical case

After performing 12 leads EKG the patients was loaded on the helicopter and directed to the cat lab where the patients arrived still pulseless but with EtCO2 38. The angio, performed after an echo showing weak heart contractility with inferior wall ipokinesia, confirmed critical occlusion of the dx coronary artery. A medicated STENT was placed with good TIMI flow result.

The patient regained consciouness a couple of hours later, and was dismissed from the hospital afer 15 days with CPC 1 and 45% EF.

In this case the strict observance of ALS protocol would have conducted the medical team to continue CPR, despite the presence of a organized rythm, due to the absence of a palpable central pulse. Epinephrine would have been regularry administered (at CA doses) and chest compressions performed.

The decision to load and go to the PCI center gave the patient the chance to treat the underlyng cause of CA.